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Abstract
Many studies have reported that regulatory T cells (CD4+CD25 + Tregs) have the potential for controlling immune pathologies, such as graft rejection and autoimmune diseases. Currently, little is known about the molecular machinery distinguishing Tregs from the CD4+CD25 - population of helper T cells (Th) cells. Foxp3, the quintessential Treg marker, may inhibit transcriptional events orchestrated by the Nuclear Factor Activating T Cells (NFAT) within the nucleus. We hypothesized that NFAT, which is present in all T cells, may be regulated differently in Tregs compared to Th cells. To address this, in vitro profiling of the pathway regulating NFAT activity was done in Tregs. These data illuminate unique aspects of NFAT regulation in Tregs. To determine if NFAT regulation had a functional role in Treg activity, the effects of NFAT inhibitors were evaluated on Treg function in vitro. Collectively, these studies support a model in which a NFAT regulation defines the transcriptional program of regulatory cells.